1. Using cultured neurons, we manipulated intracellular sodium concentrations as a marker of activity. Increased intracellular sodium caused by monensin stimulated the sodium pump to consume ATP. Immediately thereafter, transcription of mitochondrial-derived enzymes for oxidative phosphorylation was upregulated, which would lead to increased ATP synthesis. This study identified the rapid coupling mechanism between electrical activity, ATP consumption and oxidative-phosphorylation activation in mitochondria for new ATP synthesis. (Mehrabian et al 2005). 2. As a model for heart sympathetic denervation in Parkinson disease, rats were sympathetically denervated with 6-hydroxydopamine (6-OHDA). Extending our in vivo model for the brain, we measured incorporation of palmitic and arachidonic acids into phospholipids of denervated and normal hearts. Incorporation of palmitic acid (from the acyl-CoA precursor pool) was unchanged, whereas incorporation of arachidonic acid was reduced by 70%, accompanied by a reduction in phospholipase A2 activity. It now would be of interest to see if Parkinson disease patients have this denervation defect, using positron emission tomography. (Patrick et al 2005)